The broad aims of this proposal are to elucidate the role of triglyceridecontaining lipoproteins in experimentally produced atheromatosis. Cholesterol influx from chylomicron and chylomicron remnants into rabbit aorta will be compared to that of low density lipoprotein cholesterol. The role of lipoprotein receptors and of endocytosis will be examined. Similar studies in subhuman primates and in cell culture systems will also be pursued. The properties of cholesteryl ester exchange protein in human plasma will be studied and its role in the transfer of cholesteryl ester between lipoproteins with each other and between lipoproteins and cells will be investigated. Studies on lesion progression beyond the fatty streak stage will be performed by combining mechanical injury to the artery with diet modifications.